s02 spinal cord injury update-edited · conus medullaris syndrome • loss of bowel or bladder...
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Spinal Cord Injury
Robert Morgan, MD
Original Author: Mitch Harris, MD; March 2004New Author: Michael J. Vives, MD; Revised January 2006
Updated Author: Robert Morgan, MD; Revised November 2010
Overview
• Epidemiology• Pathophysiology• Classification of SCI’s & descriptive
terms• Natural History & functional prognosis• Treatment Strategies
Spinal Cord Injuryepidemiology
• Incidence: 10-12,000/ yr• 80-85% males (usually 16-30 y/o), 15-
20% female• 50% of SCI’s are complete• 50-60% of SCI’s are cervical• Immediate mortality for complete
cervical SCI ~ 50%
Spinal Cord Injuryepidemiology
– Cause• MVC 42%• Fall 20%• GSW 16%
– Gender• Male 81%• Female 19%
– Level of Education• To 8th Grade: 10%• 9th to 11th: 26%• High School: 48%• College: 16%
Etiology of SCI by Age
Source: National Spinal Cord Injury Statistical Center, University of Alabama at Birmingham, 2004 Annual Statistical Report, June, 2004
Source: National Spinal Cord Injury Statistical Center, University of Alabama at Birmingham, 2004 Annual Statistical Report, June, 2004
Employment Status
Source: National Spinal Cord Injury Statistical Center, University of Alabama at Birmingham, 2004 Annual Statistical Report, June, 2004
Percent Employed
Spinal Cord Injurypathophysiology
Primary injury• Initial insult to cord
• Local deformation
• Energy transformation
Spinal Cord Injurypathophysiology
Secondary injury
• Biochemical cascade
• Cellular processes
Most acute therapies aim to limit secondary injury cascade
Secondary Injurytheories
• 1970’s: free radicals
• 1980’s: Ca, opiate receptors lipid peroxidation
• 1990/2000’s: apoptosis intracellular protein synthesis glutaminergic mechanisms
Secondary Injury Cascadecurrent understanding
DefinitionsSpinal shock:• transient flaccid paralysis• areflexia (including bulbocavernosus reflex)• while present (usually <48 h), unable to predict
potential for neurological recovery.Neurogenic Shock:• Loss of sympathetic tone, vasomotor and
cardiac regulation.• Hypotension with relative bradycardia.
Classification
Complete• absence of sensory & motor function in lowest
sacral segment after resolution of spinal shock
Incomplete• presence of sensory & motor function in lowest
sacral segment (indicates preserved function below the defined neurological level)
ASIA Examination
Motor level (MLI) = lowest normal level with 3/5 strength (& level above = 5/5)
Each muscle has 2 root innervations, 3/5 strength = full innervation by the more rostral root level.
(4/5 acceptable with pain, de-conditioning)
• Motor Index Score (MIS) = total 100 pts • **Superiority of Motor level versus Sensory Level
Neurologic Examination
• American Spinal Injury Association (ASIA)– A = Complete – No Sacral Motor / Sensory – B = Incomplete – Sacral sensory sparing – C = Incomplete – Motor Sparing (<3) – D = Incomplete – Motor Sparing (>3) – E = Normal Motor & Sensory
ASIA Sensory Exam
– 28 sensory “points” (within dermatomes) – Test light touch & pin-prick pain
**Importance of sacral pin testing** – 3 point scale (0,1,2) – “optional”: proprioception & deep pressure to
index and great toe (“present vs absent”) – deep anal sensation recorded “present vs absent”
Motor Examination
• 10 “key” muscles (5 upper & 5 lower extremity)
C5-elbow flexion L2-hip flexion C6-wrist extension L3-knee extension C7-elbow extension L4-ankle dorsiflexion C8-finger flexion L5-toe extension T1-finger abduction S1-ankle PF
– Sacral exam: voluntary anal contraction (present/absent)
Motor Grading Scale
• 6 point scale (0-5) …..(avoid +/-’s) – 0 = no active movement – 1 = muscle contraction – 2 = active movement without gravity – 3 = movement thru ROM against gravity – 4 = movement against some resistance – 5 = movement against full resistance
ClassificationIncomplete SCI syndromes
Central Cord Syndrome• Motor loss UE>LE• Hands affected• Common in elderly w/
pre-existing spondylosis and cervical stenosis.
• Substantial recovery can be expected.
ClassificationIncomplete SCI syndromes
Brown Sequard• Ipsilateral motor,
proprioception loss.• Contralateral pain,
temperature loss.• Penetrating injuries.• Good prognosis for
ambulation.
ClassificationIncomplete SCI syndromes
Anterior Cord Syndrome• Motor loss• Vibration/position
spared• Flexion injuries• Poor prognosis for
recovery
ClassificationIncomplete SCI syndromes
Posterior Cord Syndrome
• Profound sensory loss.
• Pain/temperature less affected.
• Rare.
ClassificationOther SCI syndromes
Conus Medullaris Syndrome• Loss of bowel or bladder function• Saddle anaesthesia• Looks like cauda equina• Skeletal injuries T11-L2
Expected NeurorecoveryComplete Tetraplegia
• Little chance for functional motor recovery in LE’s
• extent of neurorecovery in UE’s determines functional independence
Expected NeurorecoveryComplete Tetraplegia
• 70-85% chance of gaining at least one additional level
• Motor grade 2/5 for a given level @1 week, all gained functional strength at next level
Ditunno, Arch Phys Med Rehabil, 2000
Expected NeurorecoveryIncomplete Tetraplegia
• >90% gain at least one UE motor level
• If pinprick spared in same dermatome, 92% chance of recovery to 3/5 motor strength
Poynton, JBJS-Br, 1997Ditunno, Arch Phys Med Rehabil, 2000
Expected NeurorecoveryIncomplete Tetraplegia
• Majority of improvement in first 6-9 months.
Waters, J Spinal Cord Med, 1998
Despite the Medical Advances of the last 50 years,
Prediction of Functional Capacity Based on Neurologic Level is still
similar to that described in:
Long, Lawton, Arch Phys Med Rehab, 1955
Functional CapacityC1-C4
• C1-C3 need mechanical ventilation (portable vent or phrenic nerve stimulator)
• C4 may need CPAP or Bi-PAP for nocturnal hypoventilation
Functional CapacityC1-C4
• Dependent for self-care and transfers.• Motorized wheelchair with special
controls- mouthsticks (C3-C4)- infrared- sip-and-puff
Functional CapacityC5
• Active elbow flexion present
• Capable of some simple ADL’s with appropriate setup:
-Eat with balanced forearm orthosis.-Write and type with opponens splint.
• Still dependent for transfers % bed positioning
Functional CapacityC6
• Added shoulder stability due to rotator cuff innervation.
• Active wrist extension (extensor carpi radialis).
• Tenodesis grip: passive finger flexion and thumb opposition with wrist extension.
• Tenodesis grip strengthened with flexor-hinge orthosis.
Functional CapacityC6
• Improved capability for self -feeding.• Self-catheterization (males), bowel
programs required.• Upper body dressing possible.• Lower body dressing difficult.• Assistance for transfers, bed mobility.• Manual wheelchair for short distances.
• Functional strength in triceps.• Can roll over, move in seated position,
transfer.• Can eat independently (except cutting).• Long distance manual wheelchair
propulsion.
Functional CapacityC7
Functional CapacityC8-T1
• Intrinsic hand function.• Improved grasp and dexterity.• Independent bed mobility & transfers.• Independent for ADL’s.
Functional CapacityThoracic Paraplegia
• Abdominal strength beginning at T6.• Sitting balance improved.• Bipedal ambulation with KAFO &
walker (swing-to gait pattern).• Energy consuming, difficult for
community use.
Ambulation after SCIMotor Requirements
• Grade 3/5 strength in hip flexors on one side
• Grade 3/5 strength in quadriceps on other side
Ambulation after SCIIncomplete Injuries
Community ambulators @ 1 year:46% of incomplete tetraplegics76% of incomplete paraplegics
Waters, Arch Phys Med Rehabil, 1994
Treatment Strategies(current & future)
Acute Stage Therapies:
– Optimize critical care management
– Modulate the secondary injury cascade
– Includes steroids, Sygen, hypothermia
Treatment Strategies(current & future)
Subacute Stage Therapies
• Modify the environment of adult CNS which inhibits neural tissue recovery.
• Includes peripheral nerve grafts, olfactory ensheathing cells, activated macrophages.
Optimize Critical Care Management• Acute respiratory failure has been observed
in patients after external immobilization for displaced odontoid fractures.
• 32 patients with posteriorly displaced fractures, 13 experienced acute respiratory compromise, whereas only one of 21 patients with anteriorly displaced fractures had respiratory difficulties (p = 0.0032).
– All 13 were initially managed using flexion traction for reduction of these fractures.
• Two of these patients died because of failure to emergently secure an airway during closed treatment of the fracture.
• Frequent respiratory deterioration during acute closed reduction of posteriorly displaced Type II odontoid fractures was observed, whereas respiratory failure in patients with anteriorly displaced fractures was rare.
• Manage the airway!
Closed management of displaced Type II odontoid fractures: more frequent respiratory compromise with posteriorly displaced fractures.
Przybylski GJ, Harrop JS, Vaccaro AR. Neurosurg Focus. 2000 Jun 15;8(6):e5.
Myth of Myelopathy• No clear case of spinal cord injury
after direct laryngoscopy in English language literature
– McLeod and Calder Criteria• All airway maneuvers cause some
motion at fracture site– Lessened with manual in line
immobilization– Increased with increasing
instability• Fiberoptic intubation minimizes
displacements– May still require direct
laryngoscopy– May require surgical airway
Crosby, E. Airway Management in Adults After Cervical Spine Trauma. Anaesthesiology. 2006
Incidence and Clinical Predictors For Tracheostomy After Cervical Spinal Cord Injury:
A National Trauma Databank Review.• After CSCI, a fifth of patients will
require tracheostomy.• Intubation on scene or ED,
complete CSCI at C1-C4 or C5-C7 levels, ISS >/=16, facial fracture, and thoracic trauma were independently associated with the need for tracheostomy.
• Patients requiring tracheostomy had a higher Injury Severity Score (ISS) and required intubation more frequently on scene and Emergency Department (ED)
• Patients requiring tracheostomy had higher rates of complete CSCI at C1-C4 and C5-C7 levels
• Patients requiring tracheostomy had more ventilation days, longer intensive care unit and hospital lengths of stay, but lower mortality.
Branco BC, Plurad D, Green DJ, Inaba K, Lam L, Cestero R, Bukur M, Demetriades D.J Trauma. 2010 Jun 3. [Epub ahead of print]
Breathing• Of patients with CSCI above C5, 87.5 per
cent required intubation compared with 61 per cent of patients with CSCI at C5-C8 (P = 0.026).
• Similarly, of patients with complete quadriplegia, 90 per cent required intubationcompared to 48.5 per cent of patients with incomplete quadriplegia or paraplegia (P < 0.001).
• There were 3 independent risk factors for the need of intubation:
– Injury Severity Score > 16– CSCI higher than C5– complete quadriplegia.
• The combination of the 2 latter risk factors resulted in intubation in 21 of 22 patients (95%).
• The majority of patients with CSCI require intubation.
• In patients with CSCI above C5 and complete quadriplegia, intubation should be offered routinely and early because delays may cause preventable morbidity.
Intubation after cervical spinal cord injury: to be done selectively or routinely?
Velmahos GC, Toutouzas K, Chan L, Tillou A, Rhee P, Murray J, Demetriades D. Am Surg. 2003 Oct;69(10):891-4.
Circulation• Early appropriate fluid
resuscitation is necessary to maintain tissue perfusion
– Avoid fluid overload!• Appropriate resuscitation
endpoint and optimal mean arterial blood pressure for maintenance of spinal cord perfusion are not known
– Uncontrolled studies using vasopressin to maintain a MAP of 85 for 7 days have shown improved outcomes
Steroidsmethylprednisolone sodium succinate
• Large body of animal studies
• Various neuroprotective mechanisms postulated
Neuroprotection w/ MPSS
Inhibition of Lipid Peroxidation
Preservation ofSpinal Cord Blood Flow
Preservation ofAerobic Metabolism
Attenuation of delayedGlutamate release
Preservation of Na, K Homeostasis
Inhibition ofCalpain-mediatedCytoskeletal damage
Preservation ofCalcium Homeostasis
National Acute Spinal Cord Injury Studies
NASCIS II• 10 hospitals, 487 patients• Compared:
MPSS (30 mg/kg bolus + 5.4 mg/kg x 23°)Naloxone (5.4 mg/kg bolus + 4.5mg/kg x 23°)Placebo
• 8 hours, steroids neurologic improvement
• Infections, PE but not significant
NASCIS III• 16 hospitals, 499 patients• 3 treatment arms (all got MPSS
bolus)MPSS 5.4 mg/kg 24 hrsMPSS 5.4 mg/kg 48 hrsTirilazad 2.5 mg/kg Q6 hr for 48 hrs
• 48 hr protocol better than 24 hr protocol (if treated between 3 and 8 hours)
• 2x incidence of pneumonia, sepsis in 48 hr group (NS)
Bracken, N Engl J Med, 1990Bracken, N Engl J Med, 1992
Bracken, JAMA, 1997Bracken, J Neurosurg, 1998
Criticism of NASCIS II• All primary outcomes (-)(no diff in neuro improvement between
grps)• (+) findings only in post-hoc
analyses(arbitrary stratification to before or
after 8hrs)• Only 38% of original enrollment
included• <8 hr control group poor results• Treatment effect small• Inappropriate statistics
60 t-testsno correctionParametric
• 6 mo results reported in media • Prior to peer-review publication• 1 yr results less encouraging
Criticism of NASCIS III• Primary outcomes negative(no diff in treatment among
groups)• all positive findings in post
hoc analyses(when arbitrarily divided into
<3hr/ >3 hr)• Treatment effects small• Effect NS @ 1yr• ? Inappropriate statistics
SYGEN®
• Monosialotetrahexosylganglioside GM1 sodium salt
• Found in CNS cell membranes
SYGEN®
experimental models• Acute
neuroprotection• Anti-excitotoxic• Potentiates neuritic
sprouting
• Single center trial, 37 pts: promising
• Multicenter trial, 800 pts: disappointing
Roisen, 1981Agnati, 1983Toffano, 1983Fass, 1984Schneider, 1998
Geisler, N Engl J Med, 1991Geisler, Spine, 2001
Acute Neuroprotective Agentsnew areas of interest in household drugs
minocycline
erythropoietin
Lipitor
Pharmacologic Neuroprotection in Patients with SCI
• No clinical evidence exists to definitively recommend the use of any neuroprotective pharmacologic agent, including steroids, in the treatment of acute SCI to improve functional recovery. (Scientific evidence–NA; Grade of recommendation–NA; Strength of panel opinion–5)
• If it has been started, stop administration of methylprednisolone as soon as possible in neurologically normal patients and in those whose prior neurologic symptoms have resolved to reduce deleterious side effects. (Scientific evidence–NA; Grade of recommendation–NA; Strength of panel opinion–5)
Subacute Stage Therapiesmodify environment of adult spinal cord
Augmentation of Regenerative Ability of CNS NeuronsNeurotrophic Factors
• Epidermal growth factor
• Fibroblast growth factor 2
• BDGF: brain derived growth factor
• Cyclic AMP
Kojima, J Neurotrauma, 2002
Inhibitors of Neurite Outgrowth
• ECM molecules in CNS myelin
• Glial scar/ cystic cavity that forms at injury site
Jones, J Neuroscience, 2002
Cellular substrates
• Bridge the gap across cystic cavity glial scar.
• Facilitate axonal regeneration in the face of various inhibitors.
Peripheral NervesRat Model
• Multiple intercostal nerve grafts
• Stabilized w/ fibrin glue & FGF
• Redirect white matter proximal togray matter distal
Cheng, Olsen, Science, 1996
Olfactory-ensheathing glial cells
• Unique ability to regenerate in adults
• “Escort” axons across CNS-PNS boundary
• May support axonal regeneration after SCI
Stem Cell Therapy
• Ongoing studies of adult mesenchymal stem cell therapy
• Animal studies are promising
• Human trials are lacking
Activated MacrophagesMacrophages play an important role in the successful regeneration of injured peripheral nerves by clearing cellular debris
Injure spinal cord of rats Extract macrophages from blood “Activate” them by exposing them to peripheral nerve Implant into spinal cord.
Activated macrophages result in significant functional recovery
Macrophages
Control
Proneuron, activated macrophages, now in clinical trials
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